Identification of gait unbalance and fallers among subjects with cerebellar ataxia by a set of trunk acceleration-derived indices of gait

Questo studio ha l’obiettivo di stabilire la capacità di 25 indicatori del cammino nel caratterizzare l’instabilità della marcia ed individuare i soggetti a rischio di cadute ricorrenti tra gli individui affetti da atassia cerebellare primariamente degenerativa (pwCA), indipendentemente dalla velocità del cammino, e ricercare la loro eventuale correlazione con le variabili cliniche e cinematiche. È stata utilizzata un’unità di misurazione inerziale per l’acquisizione degli schemi di accelerazione del tronco durante il cammino di 34 pwCA e altrettanti soggetti sani accoppiati per età e velocità (HSmatched). Per ciascun partecipante ed in ogni direzione spaziale abbiamo calcolato il rapporto armonico (HR), la percentuale di ricorrenza e di determinismo, il coefficiente di variazione di lunghezza del passo, l’esponente maggiore dell’indice di Lyapunov a breve-termine (sLLE), il normalized jerk score, il log-dimensionless jerk (LDLL-A), la radice quadrata media (RMS) ed il rapporto della radice quadrata media delle accelerazioni (RMSR). Per identificare le differenze significative tra i gruppi pwCA e HSmatched sono strati eseguiti un t-test disaccoppiato o un test di Mann-Whitney. Per stabilire la capacità di caratterizzare le alterazioni del cammino nei pwCA e in chi era soggetto a cadute sono state tracciate le curve ROC (receiver operating characteristics). Sono stati identificati i punti di cutoff ottimali e sono state calcolate le probabilità post-test. I rapporti armonici (HRs) hanno mostrato di poter caratterizzare l’instabilità del cammino e i pwCA soggetti a cadute con un’elevata probabilità. Inoltre questi erano correlati con la gravità di malattia e con la durata delle fasi di appoggio, oscillazione e doppio supporto del ciclo del passo indipendentemente dalla velocità del cammino. sLLEs, RMSs, RMSRs, e LDLJ-A si sono dimostrati in grado di caratterizzare solo in minima parte l’andatura dei pwCA ma non i pazienti soggetti a cadute

Excitability of the motor cortex in patients with migraine changes with the time elapsed from the last attack

BACKGROUND: Motor-evoked potentials (MEPs) produced by single-pulse transcranial magnetic stimulation (TMS) of the motor cortex can be an objective measure of cortical excitability. Previously, MEP thresholds were found to be normal, increased, or even reduced in patients with migraine. In the present study, we determined whether the level of cortical excitability changes with the time interval from the last migraine attack, thereby accounting for the inconsistencies in previous reports. METHODS: Twenty-six patients with untreated migraine without aura (MO) underwent a MEP study between attacks. Their data were then compared to the MEP data collected from a group of 24 healthy volunteers (HVs). During the experiment, the TMS figure-of-eight coil was positioned over the left motor area. After identifying the resting motor threshold (RMT), we delivered 10 single TMS pulses (rate: 0.1 Hz, intensity: 120% of the RMT) and averaged the resulting MEP amplitudes. RESULTS: The mean RMTs and MEP amplitudes were not significantly different between the MO and HV groups. In patients with MO, the RMTs were negatively correlated with the number of days elapsed since the last migraine attack (rho = -0.404, p = 0.04). CONCLUSION: Our results suggest that the threshold for evoking MEPs is influenced by the proximity of an attack; specifically, the threshold is lower when a long time interval has passed after an attack, and is higher (within the range of normative values) when measured close to an attack. These dynamic RMT variations resemble those we reported previously for visual and somatosensory evoked potentials and may represent time-dependent plastic changes in brain excitability in relation to the migraine cycle

Efficacy of modified atkins ketogenic diet in chronic cluster headache. An open-label, single-arm, clinical trial

Introduction: Drug-resistant cluster headache (CH) is still an open clinical challenge. Recently, our group observed the clinical efficacy of a ketogenic diet (KD), usually adopted to treat drug-resistant epilepsies, on migraine. Aim: Here, we aim to detect the effect of KD in a group of drug-resistant chronic CH (CCH) patients. Materials and methods: Eighteen drug-resistant CCH patients underwent a 12-week KD (Modified Atkins Diet, MAD), and the clinical response was evaluated in terms of response (>= 50% attack reduction). Results: Of the 18 CCH patients, 15 were considered responders to the diet (11 experienced a full resolution of headache, and 4 had a headache reduction of at least 50% in terms of mean monthly number of attacks during the diet). The mean monthly number of attacks for each patient at the baseline was 108.71 (SD = 81.71); at the end of the third month of diet, it was reduced to 31.44 (SD = 84.61). Conclusion: We observed for the first time that a 3-month ketogenesis ameliorates clinical features of CCH

Short-latency afferent inhibition and somato-sensory evoked potentials during the migraine cycle: surrogate markers of a cycling cholinergic thalamo-cortical drive?

peer reviewed[en] BACKGROUND: Short-latency afferent inhibition (SAI) consists of motor cortex inhibition induced by sensory afferents and depends on the excitatory effect of cholinergic thalamocortical projections on inhibitory GABAergic cortical networks. Given the electrophysiological evidence for thalamo-cortical dysrhythmia in migraine, we studied SAI in migraineurs during and between attacks and searched for correlations with somatosensory habituation, thalamocortical activation, and clinical features. METHODS: SAI was obtained by conditioning the transcranial magnetic stimulation-induced motor evoked potential (MEP) with an electric stimulus on the median nerve at the wrist with random stimulus intervals corresponding to the latency of individual somatosensory evoked potentials (SSEP) N20 plus 2, 4, 6, or 8 ms. We recruited 30 migraine without aura patients, 16 between (MO), 14 during an attack (MI), and 16 healthy volunteers (HV). We calculated the slope of the linear regression between the unconditioned MEP amplitude and the 4-conditioned MEPs as a measure of SAI. We also measured SSEP amplitude habituation, and high-frequency oscillations (HFO) as an index of thalamo-cortical activation. RESULTS: Compared to HV, SAI, SSEP habituation and early SSEP HFOs were significantly reduced in MO patients between attacks, but enhanced during an attack. There was a positive correlation between degree of SAI and amplitude of early HFOs in HV, but not in MO or MI. CONCLUSIONS: The migraine cycle-dependent variations of SAI and SSEP HFOs are further evidence that facilitatory thalamocortical activation (of GABAergic networks in the motor cortex for SAI), likely to be cholinergic, is reduced in migraine between attacks, but increased ictally

Visual evoked potential responses after photostress in migraine patients and their correlations with clinical features

In the past few years, researchers have detected subtle macular vision abnormalities using different psychophysical experimental tasks in patients with migraine. Recording of visual evoked potential (VEP) after photostress (PS) represents an objective way to verify the integrity of the dynamic properties of macular performance after exposure to intense light. VEPs were recorded before and after PS in 51 patients with migraine (19 with aura (MA) and 22 without aura (MO) between attacks, and 10 recorded during an attack (MI)) and 14 healthy volunteers. All study participants were exposed to 30 s of PS through the use of a 200-watt bulb lamp. The P100 implicit time and N75-P100 amplitude of the baseline VEP were compared with those collected every 20 s up to 200 s after PS. VEP parameters recorded at baseline did not differ between groups. In all groups, the VEP recordings exhibited a significant increase in implicit times and a reduction in amplitude at 20 s after the PS. In migraine, the percentage decrease in amplitudes observed at 20 s after photostress was significantly lower than in healthy volunteers, in both MO and MA patients, but not in MI patients. When data for MO and MA patients were combined, the percentage of amplitude change at 20 s was negatively correlated with the number of days that had elapsed since the last migraine attack, and positive correlated with attack frequency. We showed dynamic changes of recovery of VEP after PS depending on the migraine cycle. This finding, in conjunction with those previously attained with other neuromodulatory interventions using VEPs, leads us to argue that migraine-disease-related dysrhythmic thalamocortical activity precludes amplitude suppression by PS

Neuromodulation for Chronic Daily Headache

We reviewed the literature that explored the use of central and peripheral neuromodulation techniques for chronic daily headache (CDH) treatment. Although the more invasive deep brain stimulation (DBS) is effective in chronic cluster headache (CCH), it should be reserved for extremely difficult-to-treat patients. Percutaneous occipital nerve stimulation has shown similar efficacy to DBS and is less risky in both CCH and chronic migraine (CM). Non-invasive transcutaneous vagus nerve stimulation is a promising add-on treatment for CCH but not for CM. Transcutaneous external trigeminal nerve stimulation may be effective in treating CM; however, it has not yet been tested for cluster headache. Transcranial magnetic and electric stimulations have promising preventive effects against CM and CCH. Although the precise mode of action of non-invasive neuromodulation techniques remains largely unknown and there is a paucity of controlled trials, they should be preferred to more invasive techniques for treating CDH

A ketogenic diet normalizes interictal cortical but not subcortical responsivity in migraineurs

BackgroundA short ketogenic diet (KD) treatment can prevent migraine attacks and correct excessive cortical response. Here, we aim to prove if the KD-related changes of cortical excitability are primarily due to cerebral cortex activity or are modulated by the brainstem.MethodsThrough the stimulation of the right supraorbital division of the trigeminal nerve, we concurrently interictally recorded the nociceptive blink reflex (nBR) and the pain-related evoked potentials (PREP) in 18 migraineurs patients without aura before and after 1-month on KD, while in metabolic ketosis. nBR and PREP reflect distinct brain structures activation: the brainstem and the cerebral cortex respectively. We estimated nBR R2 component area-under-the-curve as well as PREP amplitude habituation as the slope pof the linear regression between the 1st and the 2nd block of 5 averaged responses.ResultsFollowing 1-month on KD, the mean number of attacks and headache duration reduced significantly. Moreover, KD significantly normalized the interictal PREP habituation (pre: +1.8, post: -9.1, p=0.012), while nBR deficit of habituation did not change.ConclusionsThe positive clinical effects we observed in a population of migraineurs by a 1-month KD treatment coexists with a normalization at the cortical level, not in the brainstem, of the typical interictal deficit of habituation. These findings suggest that the cerebral cortex may be the primary site of KD-related modulation.Trial registrationClinicalTrials.gov NCT03775252 (retrospectively registered, December 09, 2018)

Lateral inhibition in the somatosensory cortex during and between migraine without aura attacks. Correlations with thalamocortical activity and clinical features

BACKGROUND: We studied lateral inhibition in the somatosensory cortex of migraineurs during and between attacks, and searched for correlations with thalamocortical activity and clinical features. PARTICIPANTS AND METHODS: Somatosensory evoked potentials (SSEP) were obtained by electrical stimulation of the right median (M) or ulnar (U) nerves at the wrist or by simultaneous stimulation of both nerves (MU) in 41 migraine without aura patients, 24 between (MO), 17 during attacks, and in 17 healthy volunteers (HVs). We determined the percentage of lateral inhibition of the N20-P25 component by using the formula [(100)-MU/(M + U)*100]. We also studied high-frequency oscillations (HFOs) reflecting thalamocortical activation. RESULTS: In migraine, both lateral inhibition (MO 27.9% vs HVs 40.2%; p = 0.009) and thalamocortical activity (MO 0.5 vs HVs 0.7; p = 0.02) were reduced between attacks, but not during. In MO patients, the percentage of lateral inhibition negatively correlated with days elapsed since the last migraine attack (r = -0.510, p = 0.01), monthly attack duration (r = -0.469, p = 0.02) and severity (r = -0.443, p = 0.03), but positively with thalamocortical activity (r = -0.463, p = 0.02). CONCLUSIONS: We hypothesize that abnormal migraine cycle-dependent dynamics of connectivity between subcortical and cortical excitation/inhibition networks may contribute to clinical features of MO and recurrence of attacks